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B and T cell involvement in anti-acetylcholine receptor antibody formation in myasthenia gravis
The in vitro method of antibody production was applied to ascertain the contribution of B and T cells to the formation of anti-acetylcholine receptor (AChR) antibody. The anti-AChR antibody in the culture supernatant was estimated by radioimmunoassay, and the anti-AChR antibody-forming cells from cultures were detected by autoradiography of the antigen-binding cells. Thymic B cells from myasthenia gravis (MG) patients formed antibody when they were cultured with thymic T cells from MG patients and stimulated with AChR antigen. The antibody formation was more vigorous with thymic B cells, which contained more germinal centres. The antibody was also formed from the B and T cell combination of peripheral blood lymphocytes, although the amount was less than that produced by thymic lymphocytes from MG patients. The antibody produced by lymphocytes from MG patients. The antibody produced by lymphocytes from MG patients was suppressed by the addition of T cells from the culture supernatant of normal individuals, but not by autologous or allogeneic T cells from MG patients. The suppression by T cells from normal individuals was abolished when the cells were treated with mitomycin C. These observations indicated that AChR-specific B cells and helper T cells are active, while the suppressor T cells, which are usually present in normal individuals, are defective in MG patients.
The in vitro method of antibody production was applied to ascertain the contribution of B and T cells to the formation of anti-acetylcholine receptor (AChR) antibody. The anti-AChR antibody in the culture supernatant was estimated by radioimmunoassay, and the anti-AChR antibody-forming cells from cultures were detected by autoradiography of the antigen-binding cells. Thymic B cells from myasthenia gravis (MG) patients formed antibody when they were cultured with thymic T cells from MG patients and stimulated with AChR antigen. The antibody formation was more vigorous with thymic B cells, which contained more germinal centres. The antibody was also formed from the B and T cell combination of peripheral blood lymphocytes, although the amount was less than that produced by thymic lymphocytes from MG patients. The antibody produced by lymphocytes from MG patients. The antibody produced by lymphocytes from MG patients was suppressed by the addition of T cells from the culture supernatant of normal individuals, but not by autologous or allogeneic T cells from MG patients. The suppression by T cells from normal individuals was abolished when the cells were treated with mitomycin C. These observations indicated that AChR-specific B cells and helper T cells are active, while the suppressor T cells, which are usually present in normal individuals, are defective in MG patients.
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